ArticleJournal of virology2006
African swine fever virus causes microtubule-dependent dispersal of the trans-golgi network and slows delivery of membrane protein to the plasma membrane.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- New perspective on African swine fever: a bibliometrics study and visualization analysis.Frontiers in veterinary science · 2023Pooled it
- African swine fever virus impairs porcine alveolar macrophages bactericidal function by disrupting lysosomal acidification and cathepsin activity.PLoS pathogens · 2026Article
- Immunoevasion strategies for African swine fever virus: Modulation of antigen presentation pathways.Virulence · 2025Review
- Exploring antiviral strategies to combat African swine fever.FEMS microbiology reviews · 2025Review
- Review
- Article
- African Swine Fever Virus Host-Pathogen Interactions.Sub-cellular biochemistry · 2023Article
- African Swine Fever Virus MGF110-7L Induces Host Cell Translation Suppression and Stress Granule Formation by Activating the PERK/PKR-eIF2α Pathway.Microbiology spectrum · 2022Article
- Adaptive Cellular Immunity against African Swine Fever Virus Infections.Pathogens (Basel, Switzerland) · 2022Review
- Selective fragmentation of the trans-Golgi apparatus by Rickettsia rickettsii.PLoS pathogens · 2020Article
- Redistribution of Endosomal Membranes to the African Swine Fever Virus Replication Site.Viruses · 2017Article
- Article
- Article
- Immune regulation and evasion of Mammalian host cell immunity during viral infection.Indian journal of virology : an official organ of Indian Virological Society · 2013Article
- African swine fever virus-cell interactions: from virus entry to cell survival.Virus research · 2013Review
- Modulation of membrane traffic between endoplasmic reticulum, ERGIC and Golgi to generate compartments for the replication of bacteria and viruses.Seminars in cell & developmental biology · 2009Review
- Immune evasion during foot-and-mouth disease virus infection of swine.Immunological reviews · 2008Review
- Inhibition of the secretory pathway by foot-and-mouth disease virus 2BC protein is reproduced by coexpression of 2B with 2C, and the site of inhibition is determined by the subcellular location of 2C.Journal of virology · 2007Article
- A guide to viral inclusions, membrane rearrangements, factories, and viroplasm produced during virus replication.Advances in virus research · 2007Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral interference with secretory cargo is a common mechanism for pathogen immune evasion. Selective down regulation of critical immune system molecules such as major histocompatibility complex (MHC) proteins enables pathogens to mask themselves from their host. African swine fever virus (ASFV) disrupts the trans-Golgi network (TGN) by altering the localization of TGN46, an organelle marker for the distal secretory pathway. Reorganization of membrane transport components may provide a mechanism whereby ASFV can disrupt the correct secretion and/or cell surface expression of host proteins. In the study reported here, we used the tsO45 temperature-sensitive mutant of the G protein of vesicular stomatitis virus to show that ASFV significantly reduces the rate at which the protein is delivered to the plasma membrane. This is linked to a general reorganization of the secretory pathway during infection and a specific, microtubule-dependent disruption of structural components of the TGN. Golgin p230 and TGN46 are separated into distinct vesicles, whereupon TGN46 is depleted. These data suggest that disruption of the TGN by ASFV can slow membrane traffic during viral infection. This may be functionally important because infection of macrophages with virulent isolates of ASFV increased the expression of MHC class I genes, but there was no parallel increase in MHC class I molecule delivery to the plasma membrane.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.